Fire-Retardant, Stable-Cycling and High-Safety Sodium Ion Battery.

The safety of energy storage equipment has always been a stumbling block to the development of battery, and sodium ion battery is no exception. However, as an ultimate solution, the use of non-flammable electrolyte is susceptible to the side effects, and its poor compatibility with electrode, causing failure of batteries. Here, we report a non-flammable electrolyte design to achieve high-performance sodium ion battery, which resolves the dilemma via regulating the solvation structure of electrolyte by hydrogen bonds and optimizing the electrode-electrolyte interphase. The reported non-flammable electrolyte allows stable charge-discharge cycling of both sodium vanadium phosphate@hard carbon and Prussian blue@hard carbon full pouch cell for more than 120 cycles with a capacity retention of >85 % and high cycling Coulombic efficiency (99.7 %).

Adiponectin polymorphisms and non-alcoholic fatty liver disease risk: a meta-analysis.

BACKGROUND AND AIM: The adiponectin polymorphism has been implicated in susceptibility to non-alcoholic fatty liver disease (NAFLD), but the results remain inconclusive. The aim of this meta-analysis is to investigate the association between adiponectin polymorphisms and NAFLD risk. METHODS: All eligible case-control studies published up to September 2013 were identified by searching PubMed, Web of Science, and CNKI. Effect sizes of odds ratio (OR) and 95% confidence interval (95% CI) were calculated by using a fixed- or random-effect model. RESULTS: A total of 10 case-control studies were included; of those, there were nine studies (1223 cases and 1580 controls) for +45T>G polymorphism, seven studies (876 cases and 989 controls) for +276G>T polymorphism, and three studies (299 cases and 383 controls) for -11337C>G polymorphism. Overall, a significantly increased risk was found for +45T>G and -11377C>G polymorphism (+45T>G: OR = 1.45, 95% CI: 1.06-2.00 for recessive model, OR = 1.48, 95% CI: 1.07-2.06 for GG vs TT; -11377C>G: OR = 1.52, 95% CI: 1.10-2.09 for dominant model, OR = 3.88, 95% CI: 1.29-11.68 for GG vs CC), while for +276G>T polymorphism, we found a significantly decreased risk between them (OR = 0.65, 95% CI: 0.45-0.94 for recessive model, OR = 0.58, 95% CI: 0.40-0.84 for TT vs GG). In subgroup analysis by ethnicity, significant association was detected among Asians for +276G>T polymorphism, but not for +45T>G polymorphism. Besides, none of the three adiponectin polymorphisms was associated with the serum adiponectin levels. CONCLUSION: This meta-analysis suggests that adiponectin +45T>G and -11377C>G polymorphisms might be a risk factor for NAFLD, while +276G>T polymorphism may be a protective factor for NAFLD among Asians.

[Recurrence pattern of histological node-negative squamous cell carcinoma of the thoracic esophagus after extended radical esophagectomy with lymphadenectomy].

OBJECTIVE: To analyze the clinical and pathologic influencing factors of early recurrence in patients with histological node-negative (pN0 stage) esophageal squamous cell carcinoma after radical esophagectomy. METHODS: A retrospective study on 112 consecutive pN0 stage esophageal squamous cell carcinoma patients who underwent esophagectomy with lymphadenectomy by the same surgical team from January 2004 to December 2010. There were 92 male and 20 female patients, aging from 36 to 80 years with a mean age of 60.3 years. The Cox proportional hazards model was used to determine the independent risk factors for recurrence within 3 years after the operation. RESULTS: Recurrence was recognized in 45 patients (40.2%) within 3 years after operation. The median time to tumor recurrence was 17.4 months. Locoregional recurrence was found in 38 patients (33.9%), and hematogenous metastasis in 7 patients (6.3%). Recurrence closely correlated with tumor location, grade of differentiation, pT stage and pathologic stage (χ(2) = 6.380 to 18.837, P < 0.05). The Cox multivariate analysis showed that tumor location (RR = 1.092, P = 0.049) and pT3-4a stage (RR = 3.296, P = 0.017) were independent risk factors for postoperative locoregional recurrence. CONCLUSIONS: The most common recurrence pattern of patients with pN0 esophageal squamous cell carcinoma would develop recurrence within 3 years after operation is locoregional recurrence. Upper/middle thoracic location and pT3-4a stage are independent risk factors for locoregional recurrence of pN0 esophageal squamous cell carcinoma after operation.

[Judging the postoperative lymph node metastasis of esophagus cancer patients with pN0 stage by detecting MTA1 protein expression].

OBJECTIVE: To investigate the feasibility for judging the postoperative lymph node metastasis of esophagus cancer patients with pN0 stage by detecting the protein expression of metastasis-associated protein 1 (MTA1). METHODS: Immunohistochemistry was used to detect the expression of MTA1 protein in lymph node of esophageal squamous cell carcinoma (ESCC) with pN0 stage. RESULTS: (1) There were no significant differences in age, gender and differentiation among the lymph node metastasis (P > 0.05), but not with pT stage (P < 0.05; χ(2) = 13.29). (2) There were no significant differences among the expression of MTA1 protein and age, gender and differentiation (P > 0.05), but not with differentiation and pT stage (P < 0.05; χ(2) = 18.61). Both stages pT1b and pT3 had higher expression of MTA1 protein than stage pT1a (P < 0.05; χ(2) = 25.54). (3) The curve of lymph node metastasis showed that the patients with no/lower MTA1 protein expression had a lower metastasis rate than those a higher MTA1 protein expression (P < 0.05; χ(2) = 16.63). (4) The results of multivariate analysis confirmed that T status and MTA1 protein over-expression were independent risk factors for pN0 stage ESCC. CONCLUSION: Detecting MTA1 protein expression is helpful for judging the lymph node metastasis of ESCC patients with pN0 stage. And its over-expression may used as a guide in the decision-making of postoperative adjuvant therapy.

High-Voltage, Highly Reversible Sodium Batteries Enabled by Fluorine-Rich Electrode/Electrolyte Interphases.

High energy density and long-term cycling stability are crucial factors for the commercialization of sodium batteries in large scale. In this regard, cathode materials that can operate at high voltage have attracted great interest owing to their high energy density. However, traditional electrolytes cannot be used in high-voltage sodium batteries due to their limited oxidative stability. Therefore, there is a great challenge to develop appropriate electrolytes for high-voltage cathode materials. Herein, a diluted fluoroethylene carbonate (FEC)-based electrolyte (1 m NaPF6 in FEC/DMC = 2/8 by volume) is designed for Na4 Co3 (PO4 )2 P2 O7 (NCPP) cathode with a high operation voltage of 4.7 V to achieve superior electrochemical performance with a capacity retention of 90.10% after 500 cycles at 0.5 C and capacity retention of 89.99% after 1000 cycles at 1 C. The excellent electrochemical performance of the NCPP||Na cells can be attributed to the formation of inorganic and robust NaF-rich cathode electrolyte interphase and F-rich solid electrolyte interface on high voltage NCPP cathode and Na metal anode, respectively. This work points out a very promising strategy to develop high-voltage sodium batteries toward practical applications.

Activation of Nrf2 by miR-152 Inhibits Doxorubicin-Induced Cardiotoxicity via Attenuation of Oxidative Stress, Inflammation, and Apoptosis.

Doxorubicin (DOX) could trigger congestive heart failure, which largely limited the clinical use of DOX. microRNAs (miRNAs) were closely involved in the pathogenesis of DOX-induced cardiomyopathy. Here, we aimed to investigate the effect of miR-152 on DOX-induced cardiotoxicity in mice. To study this, we used an adeno-associated viral vector to overexpress miR-152 in mice 6 weeks before DOX treatment, using a dose mimicking the concentrations used in the clinics. In response to DOX injection, miR-152 was significantly decreased in murine hearts and cardiomyocytes. After DOX treatment, mice with miR-152 overexpression in the hearts developed less cardiac dysfunction, oxidative stress, inflammation, and myocardial apoptosis. Furthermore, we found that miR-152 overexpression attenuated DOX-related oxidative stress, inflammation, and cell loss in cardiomyocytes, whereas miR-152 knockdown resulted in oxidative stress, inflammation, and cell loss in cardiomyocytes. Mechanistically, this effect of miR-152 was dependent on the activation of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) in response to DOX. Notably, Nrf2 deficiency blocked the protective effects of miR-152 against DOX-related cardiac injury in mice. In conclusion, miR-152 protected against DOX-induced cardiotoxicity via the activation of the Nrf2 signaling pathway. These results suggest that miR-152 may be a promising therapeutic target for the treatment of DOX-induced cardiotoxicity.

[Effects on lymphangiogenesis and angiogenesis of lung cancer with antisense oligonucleotides of vascular endothelial growth factor C].

OBJECTIVE: To investigate the effects on lymphangiogenesis and angiogenesis of orthotopic implantation of lung cancer in nude mice with antisense oligonucleotides of VEGF-C. METHODS: The model in nude mice was established with orthotopic implantation for the human lung cancer cell line A549. Thirty nude mice were randomized into three groups: PBS control group, sense oligonucleotides control group and antisense oligonucleotides group (AODN group). After treatments were completed, the expression of VEGF-C and lymphatic microvessel density (LMVD) and microvessel density (MVD) of lung cancer were detected by RT-PCR,Western Blot and immunohistochemistry. RESULTS: The expression of VEGF-C in AODN group was inhibit significantly (P < 0.05). The LMVD in AODN group was decreased significantly (P < 0.1). Though the MVD in AODN group was also decreased, but there were no significant differences compared with control groups (P > 0.05). CONCLUSIONS: The antisense oligonucleotides of VEGF-C can inhibit the expression of VEGF-C in nude mice of orthotopic implantation of lung cancer. It could inhibit the lymphangiogenesis.

High glucose contributes to the proliferation and migration of non-small cell lung cancer cells via GAS5-TRIB3 axis.

Despite the growing number of studies exhibited an association of diabetes mellitus (DM) and lung cancer progression, the concrete mechanism of DM aggravating lung cancer has not been elucidated. This study was to investigate whether and how high glucose (HG) contribute to the proliferation and migration of non-small cell lung cancer (NSCLC) cells in vitro. In the present study, we confirmed that HG promoted the proliferation and migration of NSCLC cells, and also induced an anti-apoptosis effect on NSCLC cells. Moreover, HG inhibited the expression of GAS5 in NSCLC cells but elevated the protein level of TRIB3. GAS5 overexpression promoted the degradation of TRIB3 protein by ubiquitination and inhibited the HG induced-proliferation, anti-apoptosis and migration of NSCLC cells. Importantly, TRIB3 overexpression reversed the effects of GAS5 on the HG-treated NSCLC cells. Taken together, down-regulated GAS5 by HG significantly enhanced the proliferation, anti-apoptosis and migration in NSCLC cells through TRIB3, thus promoting the carcinogenesis of NSCLC.

Thymoquinone inhibits proliferation in gastric cancer via the STAT3 pathway in vivo and in vitro.

AIM: To elucidate the mechanism of thymoquinone (TQ)-induced apoptosis in human gastric cancer cells in vitro and in vivo. METHODS: HGC27, BGC823, and SGC7901 cells were cultured in vitro and treated with TQ (0, 10, 25, 50, 75, 100, 125 µmol/L) for 12 h, 24 h, and 36 h, and then the proliferation inhibitory rates were detected by methylthiazole tetrazolium assay. Apoptosis was observed after Hoechst staining. The protein expressions of signal transducer and activator of transcription (STAT)3, p-STAT3, STAT5, p-STAT5, phospho-janus-activated kinase 2 (JAK2), JAK2, p-Src, Src, glyceraldehyde-3-phosphate dehydrogenase, lamin-A, survivin, Cyclin D, Bcl-2, Bax, peroxisome proliferator activated receptor, and caspase-3,7,9 were detected by western blot. Cell cycle and apoptosis were determined with flow cytometry. TQ induced dose-dependent apoptotic cell death in HGC27 cells was measured by Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) analysis and Hoechst 33258. RESULTS: TQ inhibited the phosphorylation of STAT3 but not STAT5. TQ-induced downregulation of STAT3 activation was associated with a reduction in JAK2 and c-Src activity. TQ also downregulated the expression of STAT3-regulated genes, such as Bcl-2, cyclin D, survivin, and vascular endothelial growth factor, and activated caspase-3,7,9. Consistent with the in vitro results, TQ was significantly effective as an antitumor agent in a xenograft tumor mouse model. CONCLUSION: This study provides strong evidence that downregulation of the STAT3 signaling pathway mediates TQ-induced apoptosis in gastric cancer.

XPD Lys751Gln polymorphisms and the risk of esophageal cancer: an updated meta-analysis.

OBJECTIVE: Published data regarding the association between xeroderma pigmentosum group D XPD Lys751Gln polymorphisms and esophageal cancer (EC) cancer remain controversial. The present meta-analysis aimed to obtain a more precise estimation of the relationship between XPD Lys751Gln polymorphisms and the risk of EC. METHODS: All eligible case-control studies of Lys751Gln polymorphisms and susceptibility to EC were selected from PubMed, Web of Science and CNKI up to October 2013. The data were extracted, and pooled odds ratios (ORs) with 95% confidence intervals (CIs) were calculated. RESULTS: A total of 21 case-control studies from 19 reports were assessed in this meta-analysis, including 6,581 cases and 8,251 controls. There was a significant association between the XPD Lys751Gln polymorphism and the risk of esophageal cancer in the overall population (Dominant model: OR=1.30, 95%CI: 1.07-1.57, p<0.05; Lys/Gln vs. Gln/Gln: OR=1.20, 95%CI: 1.05-137, p<0.05; Gln/Gln vs. Lys/Lys: OR=1.76, 95%CI: 1.08-2.85, p=0.02; Recessive model: OR=1.48, 95%CI: 1.06-2.07, p=0.02). Similar results were found when stratified according to the cancer type, ethnicity and control source. However, no associations were found among smokers or drinkers. CONCLUSION: The results of this meta-analysis suggest that XPD Lys751Gln polymorphisms contribute to susceptibility to EC.

Synergistic antitumor effect of puerarin combined with 5-fluorouracil on gastric carcinoma.

Combination chemotherapy is a crucial method in the treatment of gastric cancer. The aim of the present study was to investigate the inhibitory effects of puerarin and 5­fluorouracil (5­FU) on BGC­823 gastric cancer cells in vitro and in vivo. The in vitro growth inhibition of puerarin or 5­FU alone or combined on BGC­823 cells was determined using a cell counting kit 8 (CCK­8) on living cells. Apoptotic morphological features and proteins expression levels were detected by Hoechst 33258 staining, an Annexin V/propidium iodide apoptosis kit and western blot analysis, respectively. Tumor xenografts were established in nude mice and the inhibitory effects and side effects were detected. Results of the CCK­8, Hoechst 33258 staining and flow cytometry revealed that the combined treatment was more effective than the separate treatments. The tumor volume was 90.65% of that of the controls and the mean tumor weight was only 0.125 g at the end of the experiment in the combination group compared with the control group (0.822 g). In addition, it was determined that liver and renal toxicity did not increase in combined treatment. These findings showed that puerarin and 5­FU produced a significant synergic effect on gastric cancer cells, while there was no increase in side effects.

Synergistic effect of puerarin and 5-fluorouracil on hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is one of the most common types of human malignancy worldwide, which is becoming increasingly resistant to traditional drug treatments. Puerarin combined with 5-fluorouracil (5-FU) may be a useful treatment for liver cancer. The primary aim of the present study was to determine whether combined treatment with 5-FU and puerarin is more effective against the hepatocellular carcinoma (HCC) cell line, SMMC7721, than treatment with 5-FU or puerarin alone. The growth inhibition of SMMC7721 cells by puerarin or 5-FU alone or in combination was determined by the Cell Counting Kit-8 assay, in vitro. Apoptotic morphological features and the percentage of apoptotic cells were detected using Hoechst 33258 staining and an Annexin V/PI apoptosis kit, respectively. In addition, a tumor xenograft model was established in nude mice using SMMC7721 cells. Puerarin and 5-FU alone or in combination were injected into the mice, and the inhibition of tumor growth was evaluated by monitoring tumor volume and weight. Treatment with 6,400 or 640 µM 5-FU resulted in growth inhibition of 95.56±0.81 and 75.91±3.54%, respectively. The combination index values were <1 when the fraction of affected cells was between 0.2555 and 0.7420. Furthermore, the percentage of apoptotic cells was markedly increased in the combined treatment group when compared with that of the individual treatment groups, in vitro and in vivo. Individual treatment with puerarin resulted in a tumor volume inhibition rate (IR) of 70.58% and a tumor weight IR of 46.20%. Treatment with 5-FU was found to decrease the tumor volume by 76.26% and tumor weight by 49.86%. In the combined treatment group, the tumor volume and weight IRs were 93.11 and 75.21%, respectively. A marked increase in the inhibition of tumor growth and the number of apoptotic cells in response to combined treatment with puerarin and 5-FU was identified with no observed liver or renal toxicity. These results suggest that puerarin and 5-FU exhibit a synergistic treatment effect on the HCC SMMC7721 cell line.

Synergistic effects of puerarin combined with 5-fluorouracil on esophageal cancer.

Puerarin is an isoflavone derived from kudzu roots with a wide range of biological and medicinal properties. The aim of the present study was to investigate the inhibitive effects of puerarin combined with 5­fluorouracil (5­FU) on Eca­109 esophageal cancer cells in vitro and in vivo. Inhibitive effects of the treatments on Eca­109 cells were detected by cell counting kit­8, Hoechst 33258 staining and flow cytometry. A tumor xenograft model was established in nude mice. Puerarin and 5­FU, administered either in combination or individually, were injected into mice and the inhibitive effects along with any side effects were observed. Apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Puerarin and 5­FU, administered as combined treatment or individual drugs, significantly inhibited proliferation and induced marked apoptosis. The mean growth inhibition rate (± standard deviation) reached 87.27±5.37% and the apoptotic rate at 48 h reached 36.18±1.24% in the combined treatment group. The percentages of apoptotic cells induced by puerarin and 5­FU (combined or alone) were significantly higher than those of the control group (P<0.05). Puerarin or 5­FU alone significantly inhibited the growth of xenograft tumors in comparison to the control group (P<0.05), with inhibition rates of 76.93 and 72.21%, respectively. The drugs combined exhibited a significantly greater effect than either drug alone (P<0.05), with the tumor inhibition rate reaching 89.06%. During the course of chemotherapy, no evident side effects were observed. The results suggested that the combined inhibitive effects of puerarin and 5­FU were greater than the effects of the agents used individually. In addition, puerarin combined with 5­FU exhibited synergistic effects at lower concentrations and promoted apoptosis, but did not increase the side effects of chemotherapy, which indicated that puerarin may be a safe and effective chemosensitive agent in the treatment of human esophageal cancer.

Suppressive effect of sinomenine combined with 5-fluorouracil on colon carcinoma cell growth.

It is reported that sinomenine (SIN) and 5-fluorouracil (5-FU) both are effective for colon cancer, but their cooperative suppressive effects and toxicity remain to be clarified in detail. This study aimed to determine suppressive effects and toxicity of sinomenine (SIN) plus 5-fluorouracil (5-FU) on LoVo colon carcinoma cells in vitro and in vivo. CCK-8, Hoechst 33258 staining and an annexin V-FITC/PI apoptosis kit were used to detect suppressive effects. Western blotting was applied to investigate the essential mechanism underlying SIN and 5-FU-induced apoptosis. SIN or 5-FU or both were injected into nude mice, and then suppressive effects and side effects were observed. SIN plus 5-FU apparently inhibited the proliferation of LoVo cells and induced apoptosis. Moreover the united effects were stronger than individually (p<0.05). The results of annexin V-FITC /PI staining and Hoechst 33258 staining showed that the percentage of apoptotic cells induced by SIN and 5-FU combined or alone was significantly higher than the control group (p<0.05). Expression of Bax and Bcl-2 was up-regulated and down-regulated respectively. SIN or 5-FU significantly inhibited effects on the volume of tumour xenografts and their combined suppressive effects were stronger (p<0.05). No obvious side effects were observed. It was apparent that the united effects of SIN and 5-FU on the growth of colorectal carcinoma LoVo cells in vitro and in vivo were superior to those using them individually, and it did not markedly increase the side effects of chemotherapy.

XPD Asp312Asn polymorphism and esophageal cancer risk: an update meta-analysis based on 3928 cases and 6012 controls.

BACKGROUND: Although xeroderma pigmentosum group D (XPD) was reported to be related with esophageal cancer (EC) risk, the results remained inconsistent. The aim of this meta-analysis was to make a more precise estimation of the relationship between XPD Asp312Asn polymorphism and EC risk. METHODS: We searched PubMed, Web of Science, Embase, Medline, CNKI and Chinese Biomedical database, covering all publications (up to May, 2014). Statistical analyses were performed with Stata software (version 12.0, USA) and RevMan 5.1 (Copenhagen, 2008). The calculation of odds ratios (ORs) with 95% confidence intervals (CI) was calculated to assess the strength of the association. RESULTS: A total of 15 case-control studies from 13 literatures including 3928 cases and 6012 controls described Asp312Asn genotypes and EC risk. A significant association between XPD Asp312Asn polymorphism and EC risk was found when all the eligible studies were pooled into this meta-analysis. It's also the same result in subgroup analysis of smokers in dominant model (OR=1.63, 95% CI: 1.06-2.50, P=0.03). However, in the stratified analysis by ethnicity and source of population controls, no association between them was discovered. CONCLUSION: The XPD Asp312Asn polymorphism was proved to contribute to the risk of EC in this meta-analysis. Data showed that tobacco consumption may increase the susceptibility of EC.

Clinical study on postoperative recurrence in patients with pN0 esophageal squamous cell carcinoma.

BACKGROUND: Despite increasingly radical surgery for esophageal carcinoma, many patients still develop tumor recurrence after operation. This study was designed to analyze the clinical and pathologic influencing factors of early recurrence in patients with histological node-negative (pN0 stage) esophageal squamous cell carcinoma (ESCC) after radical esophagectomy. METHODS: A retrospective study on 112 consecutive pN0 stage ESCC patients who underwent esophagectomy with lymphadenectomy by the same surgical team from January 2004 to December 2010. There were 92 male and 20 female patients, aging from 36 to 80 years with a mean age of 60.3 years. The Cox proportional hazards model was used to determine the independent risk factors for recurrence within 3 years after the operation. RESULTS: Recurrence was recognized in 45 patients (40.2%) within 3 years after operation. The median time to tumor recurrence was 17.4 months. Locoregional recurrence was found in 38 patients (33.9%) and hematogenous metastasis in 7 patients (6.3%). However, locoregional recurrence accounted for 84.4% of all relapse patients. Recurrence closely correlated with tumor location, grade of differentiation, primary tumor stage (pT) and pathologic stage (χ2 = 6.380 to 18.837, p < 0.05). The Cox multivariate analysis showed that upper/middle thoracic location (OR = 1.092, p = 0.049) and pT3-4a stage (OR = 3.296, p = 0.017) were independent risk factors for postoperative locoregional recurrence. CONCLUSION: Locoregional recurrence was the most common recurrence pattern of patients with pN0 ESCC within 3 years after operation. Upper/middle thoracic location and pT3-4a stage were independent risk factors for locoregional recurrence of pN0 ESCC after radical esophagectomy.

[Multimodality management of squamous cell carcinoma of thoracic esophagus].

Most patients with esophageal cancer have advanced disease at presentation. The efficacy of surgical resection alone is often unsatisfactory in patients with stage III or more advanced cancer according to the seventh edition of UICC staging system for esophageal cancer. The systematic multidisciplinary treatment is important. Mounting evidence indicates that preoperative concurrent chemoradiotherapy is the most effective induction therapy to down-stage tumor and increase radical resection rate. For the esophageal squamous cell carcinoma patients with multi-stations and multi-fields lymph node metastasis, preoperative induction chemotherapy would be a viable option. For locally advanced cancers which have been surgically resected, postoperative adjuvant radiotherapy maybe helpful to improve local control for the insufficient surgical dissection. The role of adjuvant chemotherapy also needs further studies. Thoracic esophageal squamous cell carcinoma and lower esophageal adenocarcinoma which is common in western countries are different. We need more prospective clinical studies to establish our treatment modalities for esophageal cancer.

Decreased EGR3 expression is related to poor prognosis in patients with gastric cancer.

The early growth response (EGR) family has a highly conserved DNA-binding domain and encodes zinc finger proteins, which show suppressive effects on tumour growth. However, the expression and significance of EGR3 in gastric cancer are still unknown. In this study, real-time PCR, immunohistochemistry and western blot assays were performed to detect the expression of EGR3 in gastric cancer tissues and matched non-tumour tissues and to further analyse the EGR3 expression associated with clinical pathological factors, including prognosis. Our results showed that EGR3 expression was significantly lower in gastric cancer tissues compared with matched non-tumour tissues and that patients with lower EGR3 expression had a poorer prognosis compared with patients with higher EGR3 expression. Our results suggest that decreased EGR3 expression might play a critical role in the differentiation, proliferation, metastasis and progression of gastric cancer cells and may also be a potential diagnostic marker for gastric cancer.

[Risk factors of recurrence and metastasis in pN1 stage squamous cell carcinoma of the thoracic esophagus after radical esophagectomy with lymphadenectomy].

OBJECTIVE: To analyze the clinical and pathologic risk factors of early recurrence in patients with pathological N1 (pN1) stage esophageal squamous cell carcinoma after radical esophagectomy. METHODS: A retrospective study was carried out on 95 consecutive pN1 stage esophageal squamous cell carcinoma patients undergoing esophagectomy with lymphadenectomy by the same surgical team from January 2004 to December 2010 was performed. The Cox proportional hazards model was used to determine the independent risk factors for recurrence and metastasis within 3 years after the operation. RESULTS: Recurrence was identified in 52 patients (54.7%) within 3 years after operation. Local recurrence was found in 42 patients (44.2%), and distant metastasis in 10 patients (10.5%). The Cox multivariate analysis showed that pT3-4a stage (RR=3.604, P=0.027), positive lymph node metastasis in two stations (RR=4.834, P=0.009) or two fields (RR=5.689, P=0.003), and postoperative adjuvant chemotherapy (RR=1.594, P=0.048) were independent risk factors for postoperative recurrence. CONCLUSIONS: Postoperative adjuvant chemotherapy can decrease the probability of postoperative recurrence and metastasis of pN1 esophageal squamous cell carcinoma. As for patients who are identified as multi-station or multi-field lymph node metastasis, preoperative induced therapy maybe further improve treatment outcomes.